OBJECTIVE: To investigate the changes of creatine kinase-MB (CK-MB) and heat shock protein 60 (HSP 60) in rats without electric marks after electric injury, to identify the relationship of the CK-MB, HSP 60 and the time of electric injuries, and to evaluate the damage to cells after electric injury. METHODS: The animal model of electric injury without electric marks was established by alternating current (voltage 110 V). Automatic biochemistry analyzer was used to detect the serum CK-MB and immunohistochemical staining technology was used to analyze the tissues of myocardium and left lobe of liver. RESULTS: The amount of serum CK-MB was increased when the rats were injuried, and reached the peak at 30min. Then the amount of CK-MB began to decrease and showed a slight downward trend in 3-5 h after electric injury, and leveled off at 6 h. Immunohistochemistry staining also showed the changes of HSP 60 of rats' myocardial cells and hepatic cells regularly after electric injury. CONCLUSION The regular changes of serum CK-MB and tissular HSP 60 in rats can be used to diagnosis electric injury and assess the injury of internal organs after the electric injury without electric marks.
Animals ; Chaperonin 60/metabolism* ; Creatine Kinase, MB Form/metabolism* ; Electric Injuries/complications* ; Immunohistochemistry ; Liver/pathology* ; Myocardium/pathology* ; Rats

We report a 43-year-old male who suffered cognitive dysfunction after an electric injury. He underwent evaluation for cognitive dysfunction and cerebral glucose hypometabolism at 1 week and 6 months. In contrast to the progressive decline of frontal lobe functions and visuospatial functions, memory and depressive mood were improved. SPM99 showed hypometabolic areas in the frontal and occipital lobes which were widened. Moreover new cingulate lesions appeared. This illustrates that the progression of derangement of cerebral glucose metabolism is correlated with neuropsychological impairment.
Adult ; Electric Injuries* ; Follow-Up Studies* ; Frontal Lobe ; Glucose ; Humans ; Male ; Memory ; Metabolism ; Neuropsychology ; Occipital Lobe ; Positron-Emission Tomography

OBJECTIVE: To study the changes of HSP 70 mRNA and c-fos mRNA expression and to find a method to differentiate antemortem from postmortem electrocution. METHODS: Fifteen New Zealand rabbits were randomly divided into three groups, the antemortem electrocution group, the postmortem electrocution group, and the control group. Each group consists of five rabbits. The levels of HSP 70 mRNA and c-fos mRNA in skeletal muscle and cardiac muscle were examined with quantitative fluorescent RT-PCR. RESULTS: The levels of HSP 70 mRNA and c-fos mRNA in the antemortem electrocution group increased significantly (P<0.05), compared with that of the postmortem electrocution group. CONCLUSION The changes of HSP 70 mRNA and c-fos mRNA expression in skeletal muscle and cardiac muscle can be used as an indicator to distinguish antemortem from postmortem electrocution.
Animals ; Electric Injuries/metabolism* ; Forensic Pathology ; HSP70 Heat-Shock Proteins/metabolism* ; Male ; Muscle, Skeletal/metabolism* ; Myocardium/metabolism* ; Postmortem Changes ; Proto-Oncogene Proteins c-fos/metabolism* ; RNA, Messenger/metabolism* ; Rabbits ; Random Allocation

OBJECTIVETo study the effects of sacral nerve root electrostimulation (SNS) on the colon function and its mechanisms in rats with spinal cord injury (SCI).

METHODSOne hundred and four Wistar rats were divided into three groups: A, B and C. A group ( n = 24) was divided into three subgroups (n = 8) for studying the bioelectricity: Normal group (NG), SCI group (SCI) and SCI group with SNS(SNS); B group( n = 24) was divided into three subgroups( n = 8) for studying the colon motility: NG, SCI and SNS. C group( n = 56) were divided into three groups for studying the change of morphology and neurotransmitters(SP and VIP): NG (n = 8), SCI (n = 24), and SNS (n = 24) . In SCI and SNS, included of three subgroups: 24, 48, 72 h after spinal cord injury (n = 8).

RESULTSIn SCI group, the activity of bioelectricity in proximal and distal colon was reduced; the colon motility was lessened, and colon mucosa appeared different degree of damage; cell-cell connections between intestinal epithelial cells were destroyed. The expressions of substance P(SP) and vasoactive intestinal peptide (VIP) in colon were decreased obviously. SNS was found to activate the bioelectricity, promote the colon motility, improve the intestinal mucosal, and increase the expressions of SP and VIP. Conclusion: SNS can activate the peristalsis, rehabilitate the motility of denervated colon, protection of the intestinal mechanical barrier between intestinal epithelial cells and tight junction, rebuild the colon function through activating the bioelectricity and increase the expressions of SP and VIP.

Animals ; Colon ; physiopathology ; Electric Stimulation Therapy ; Epithelial Cells ; drug effects ; Intestinal Mucosa ; drug effects ; Lumbosacral Region ; innervation ; Neurotransmitter Agents ; metabolism ; Rats ; Rats, Wistar ; Spinal Cord Injuries ; therapy ; Substance P ; metabolism ; Vasoactive Intestinal Peptide ; metabolism

OBJECTIVE: To study the expression of c-fos in organs after rats electrified. METHODS: The brain, lung, heart, liver, spleen, kidney, muscle of electrified limb, and cutis of electrified limb of all experimental rats and those organs of control groups were dissected to detect the expression of c-fos by using immunohistochemistry staining, and the staining intensity were assessed by image analysis system. RESULTS: The expression of c-fos was observed in brain, heart, liver, lung, kidney and muscle in electrified directly group, the amount of expression reached peak at 2 h after electrified and decreasing at 8 h after electrified, and the expression showed faintness in electrified at the immediate after death group. The expressions of c-fos in spleen and cutis is negative in all groups. The expression of c-fos in all detected organs was negative in other rats that were electrified after death. CONCLUSION c-fos can be regard as a target in identifying electrical injury, whether it formed at antemortem or postmortem.
Animals ; Brain/pathology* ; Death ; Disease Models, Animal ; Electric Injuries/pathology* ; Immunohistochemistry ; Kidney/metabolism* ; Liver/metabolism* ; Lung/pathology* ; Male ; Myocardium/pathology* ; Proto-Oncogene Proteins c-fos/metabolism* ; Rats ; Rats, Sprague-Dawley ; Staining and Labeling ; Time Factors

The present study aimed to identify which mitogen-activated protein kinase (p38 or Jun amino-terminal kinase [JNK]) was involved in cavernosal apoptosis during the acute phase after cavernosal nerve crush injury (CNCI) in rats to ameliorate apoptosis of cavernosal tissue, such as smooth muscle (SM). A total of twenty 10-week-old male Sprague-Dawley rats were divided equally into two groups: sham surgery (S) and CNCI (I). The I group approximated the clinical situation of men undergoing radical prostatectomy using two 60-second compressions of both CNs with a microsurgical vascular clamp. At 2-week postinjury, erectile response was assessed using electrostimulation. Penile tissues were harvested for immunohistochemistry analysis of alpha-SM actin (α-SMA), western blot analysis, and double immunofluorescence analysis of α-SMA and phosphorylated p38 or JNK, as well as double immunofluorescent of TUNEL and phosphorylated p38 or JNK. At 2-week postinjury, the I group had a significantly lower intracavernous pressure (ICP)/mean arterial pressure (MAP) and a lower area under the curve (AUC)/MAP than the S group. The I group also exhibited decreased immunohistochemical staining of α-SMA, an increase in the number of SM cells positive for phosphorylated JNK, an increased number of apoptotic cells positive for phosphorylated JNK, and increased JNK phosphorylation compared with the S group. However, there was no significant difference in p38 phosphorylation expression or the number of SM cells positive for phosphorylated p38 between the two groups. In conclusion, our data suggest that JNK, not p38, is involved in cavernosal apoptosis during the acute phase after partial CN damage.
Animals ; Apoptosis ; Disease Models, Animal ; Electric Stimulation ; MAP Kinase Kinase 4/metabolism* ; Male ; Penile Erection ; Penis/pathology* ; Peripheral Nerve Injuries/pathology* ; Phosphorylation ; Prostatectomy ; Rats ; Rats, Sprague-Dawley ; Signal Transduction ; p38 Mitogen-Activated Protein Kinases/metabolism*

OBJECTIVETo study the protective effects of sacral nerve root electrostimulation on intestinal mechanical barrier in rats with spinal cord injury (SCI).

METHODSFifty six Wistar rats were divided into normal group, SCI control group and SCI group with sacral nerve root electrostimulation (8 rats in each subgroup at 24, 48, 72 h after spinal cord injury). The following experiments were performed respectively in rats from the 3 groups: bacteria culture from intestinal mesentery lymph nodes, liver, spleen, intestinal morphology observation and detection the protein expression level of ZO-1.

RESULTSThe intestinal mucosa appeared different degree of damage in SCI control group; cell-cell connections between intestinal epithelial cells were destroyed; Endotoxin levels in blood and the number of bacterial translocation increased obviously. Sacral nerve stimulation was found toimprove the intestinal mucosal, reduce the endotoxin content in the blood to normal level and the decrease the incidences of bacterial translocation of the gut origin. The expression of tight junction protein ZO-1 of rat intestinal tissue had no statistical differences among the 3 groups. On the other hand, the distribution of tight junction protein ZO-1 appeared different degrees of scattered and irregular in the control group while that in the experimental group appeared different degree of improvement as determined by the immunohistochemistry of rat intestinal tissue.

CONCLUSIONsacral nerve root electrostimulation can rehabilitate the peristalsis of denervated colon, promote defeacation and decrease bacterial amount, protection of the intestinal mechanical barrier between intestinal epithelial cells and tight junction, reducing the endotoxin content in the blood and suppressing bacterial translocation from the gut.

Animals ; Bacterial Translocation ; Electric Stimulation Therapy ; Endotoxins ; blood ; Epithelial Cells ; cytology ; Intestinal Mucosa ; physiology ; Peristalsis ; Rats ; Rats, Wistar ; Spinal Cord ; Spinal Cord Injuries ; physiopathology ; Zonula Occludens-1 Protein ; metabolism

OBJECTIVETo observe the effects of low molecular weight heparin (LMWH) on the inflammatory response and vascular injury in rat after electric burn.

METHODSA homemade regulator and transformer apparatus was used to reproduce the model of electric burn (0.5 cm×0.5 cm in size) with depth from full-thickness to full-thickness skin plus muscle and bone on the middle of the inside of right hind limb in 60 Wistar rats. The open wounds were covered with 20 g/L sulfadiazine silver paste immediately after injury. The wound condition was observed every day. The injured rats were divided into group LMWH and control group (C) according to the random number table, with 30 rats in each group. Rats in group LMWH were given subcutaneous injection of LMWH (1 U/g) in abdominal wall, 2 times a day. No other treatment was given in rats in group C. On post burn day (PBD) 3, 5, and 10, 10 rats respectively of two groups were sacrificed. The damaged tissue of wound and that around the wound (1.0 cm×0.5 cm in size) were excised, and heart blood was obtained. The pathological changes and thrombosis in damaged tissue were observed with HE, Masson, and aldehyde fuchsin staining, and the thrombosis rate was calculated. Serum contents of TNF-α and endothelin-1 were determined with ELISA. The mRNA expression of TNF-α in damaged tissue was detected with RT-PCR. Data were processed with Levene homogeneity test, analysis of variance of factorial design, LSD- t test, SNK- q test, and Friedman M nonparametric test.

RESULTS(1) The injured limb of rats was obviously swollen after electric burn, which reached deeply to the muscle and bone. Compared with those of group C, the swelling of rats subsided slightly faster and the inflammatory response was lighter in group LMWH at each time point. (2) The necrosis of damaged tissue and profuse infiltration of inflammatory cells were observed. Dilatation of blood vessels, congestion and thrombosis, and swelling, necrosis, and desquamation of vascular endothelial cells were observed in the damaged tissue. Damaged blood vessel wall, ruptured elastic fiber, loss of internal elastic membrane, and other pathological changes were observed in the damaged tissue of rats in the two groups. Above lesions were improved gradually along with the passage of time, and the improvement was more obvious in rats of group LMWH compared with that of group C on PBD 5 and 10. (3) The thrombosis rates of rats in group LMWH were obviously lower than those of rats in group C (F = 4.921, P < 0.05). The thrombosis rates of rats in group LMWH on PBD 3 and 10 were respectively (0.07 ± 0.11)% and (0.03 ± 0.05)%, which were significantly lower than those of rats in group C [(0.16 ± 0.15)% and (0.13 ± 0.18)%, with t values respectively 2.17 and 2.07, P values below 0.05]. In group LMWH, the thrombosis rate of rats on PBD 10 was obviously lower than that on PBD 3 (t = 3.61, P < 0.05). (4) The serum contents of TNF-α and endothelin-1 of rats in group LMWH were significantly lower than those of rats in group C (F = 47.161, χ(2) = 81.46, P values below 0.01). In group LMWH, TNF-α contents were respectively (71 ± 24), (74 ± 14), (72 ± 20) pg/mL, and endothelin-1 contents were respectively (20.9 ± 3.2), (19.8 ± 5.2), (18.6 ± 1.1) ng/mL on PBD 3, 5, and 10, and they were significantly lower than those of rats in group C [(195 ± 148), (96 ± 20), (159 ± 46) pg/mL and (38.8 ± 15.4), (27.9 ± 3.6), (25.6 ± 7.6) ng/mL, with t values from 3.81 to 8.05, q values from 4.41 to 7.85, P < 0.05 or P < 0.01]. (5) The mRNA expression levels of TNF-α in damaged tissue of rats in group LMWH were significantly lower than those of rats in group C (F = 199.113, P < 0.01). The mRNA expression levels of TNF-α of rats in group LMWH were respectively 0.93 ± 0.10, 1.15 ± 0.12, 1.21 ± 0.11 on PBD 3, 5, and 10, and they were significantly lower than those of group C (1.68 ± 0.15, 1.43 ± 0.12, 1.50 ± 0.13, with t values from 3.75 to 6.12, P < 0.05 or P < 0.01). In group LMWH, the mRNA expression level of TNF-α of rats on PBD 10 was obviously higher than that on PBD 3 (t = 3.61, P < 0.05).

CONCLUSIONSLMWH intervention can ameliorate vascular injury and inflammatory response of electrically burned wounds in rats, and it decreases thrombosis rate in the vessels of injured limb.

Animals ; Anticoagulants ; administration & dosage ; Burns, Electric ; blood ; complications ; therapy ; Endothelin-1 ; Heparin, Low-Molecular-Weight ; administration & dosage ; Male ; Rats ; Rats, Wistar ; Serum ; metabolism ; Treatment Outcome ; Tumor Necrosis Factor-alpha ; blood ; Vascular System Injuries ; therapy

The aim of this study was to investigate the effect of platelet-rich plasma (PRP) on cavernous nerve (CN) regeneration and functional status in a nerve-crush rat model. Twenty-four Sprague-Dawley male rats were randomly divided into three equal groups: eight had a sham operation, eight underwent bilateral nerve crushing with no further intervention and eight underwent bilateral nerve crushing with an immediate application of PRP on the site of injury. Erectile function was assessed by CN electrostimulation at 3 months and nerve regeneration was assessed by toluidine blue staining of CN and nicotinamide adenine dinucleotide phosphate (NADPH)-diaphorase staining of penile tissue. Three months after surgery, in the group that underwent bilateral nerve crushing with no further intervention, the functional evaluation showed a lower mean maximal intracavernous pressure (ICP) and maximal ICP per mean arterial pressure (MAP) with CN stimulation than those in the sham group. In the group with an immediate application of PRP, the mean maximal ICP and maximal ICP/MAP were significantly higher than those in the injured control group. Histologically, the group with the application of PRP had more myelinated axons of CNs and more NADPH-diaphorase-positive nerve fibres than the injured control group but fewer than the sham group. These results show that the application of PRP to the site of CN-crush injury facilitates nerve regeneration and recovery of erectile function. Our research indicates that clinical application of PRP has potential repairing effect on CN and peripheral nerves.
Animals ; Disease Models, Animal ; Electric Stimulation ; Erectile Dysfunction ; pathology ; physiopathology ; therapy ; Male ; NADPH Dehydrogenase ; metabolism ; Nerve Regeneration ; physiology ; Penile Erection ; physiology ; Penis ; innervation ; Peripheral Nerve Injuries ; Peripheral Nerves ; metabolism ; pathology ; Platelet Transfusion ; Platelet-Rich Plasma ; Radiculopathy ; etiology ; pathology ; physiopathology ; Rats ; Rats, Sprague-Dawley

We evaluated whether LIM-kinase 2 inhibitor (LIMK2i) could improve erectile function by suppressing corporal fibrosis through the normalization of the Rho-associated coiled-coil protein kinase 1 (ROCK1)/LIMK2/Cofilin pathway in a rat model of cavernous nerve crush injury (CNCI). Sixty 11-week-old male Sprague-Dawley rats were divided equally into five groups: sham surgery (S), CNCI (I), and CNCI treated with low-dose (L), medium-dose (M), and high-dose (H) LIMK2i. The L, M, and H groups were treated with a daily intraperitoneal injection of LIMK2i (2.5, 5.0, and 10.0 mg kg^-1 body weight, respectively) for 1 week after surgery. The erectile response was assessed using electrostimulation at 1 week, postoperatively. Penile tissues were processed for Masson's trichrome staining, double immunofluorescence, and Western blot assay. Erectile responses in the H group improved compared with the I group, while the M group showed only partial improvement. A significantly decreased smooth muscle/collagen ratio and an increased content of fibroblasts positive for phospho-LIMK2 were noted in the I group. The M and H groups revealed significant improvements in histological alterations and the dysregulated LIMK2/Cofilin pathway, except for LIMK2 phosphorylation in the M group. The inhibition of LIMK2 did not affect the ROCK1 protein expression. The content of fibroblasts positive for phospho-LIMK2 in the H group returned to the level found in the S group, whereas it did not in the M group. However, the L group did not exhibit such improvements. Our data suggest that the inhibition of LIMK2, particularly with administration of 10.0 mg kg^-1 body weight LIMK2i, can improve corporal fibrosis and erectile function by normalizing the LIMK2/Cofilin pathway.
Animals ; Cofilin 1/metabolism* ; Electric Stimulation ; Erectile Dysfunction/etiology* ; Fibroblasts/pathology* ; Fibrosis/drug therapy* ; Lim Kinases/antagonists & inhibitors* ; Male ; Penile Diseases/drug therapy* ; Penis/innervation* ; Peripheral Nerve Injuries/pathology* ; Phosphorylation ; Rats ; Rats, Sprague-Dawley ; Signal Transduction/drug effects* ; rho-Associated Kinases/genetics*